HaCaT keratinocytes were transfected with the empty vector (Vec) or the RNF144A plasmid for 24 h and then treated with HSV60 (1 μg/ml), HT‐DNA (1 μg/ml), or left untreated for 8 h. The cells were lysed for real‐time PCR assays.
PMA‐THP1 cells were transfected with control siRNA (SC) or RNF144A‐specific siRNA (A2). At 24 h after transfection, the cells were transfected with HSV60 (1 μg/ml), HT‐DNA (1 μg/ml), or ISD (1 μg/ml) for 8 h. The cells were lysed for real‐time PCR assays.
PMA‐THP1 cells were transfected with control siRNA (SC) or RNF144A‐specific siRNA (A2, A3). At 24 h after transfection, the cells were transfected with poly(dA:dT) (1 μg/ml), HT‐DNA (1 μg/ml), or poly(I: C) (2.5 μg/ml) for 8 h. The cells were lysed for immunoblot assays.
Wild‐type (WT) and Rnf144a‐deficient (KO) PMA‐THP1 cells were infected with HSV‐1 (MOI = 1) for 8 h. The cells were lysed for immunoblot assays.
Wild‐type (WT) and Rnf144a‐deficient (KO) PMA‐THP1 cells were infected with HSV‐1 (MOI = 1) for 24 h. The supernatants were collected and subjected to ELISA assays.
Wild‐type (WT) and Rnf144a‐deficient (KO) PMA‐THP1 cells were infected with HSV‐1 (MOI = 1) for the indicated periods. The cells were lysed for real‐time PCR assays.
Wild‐type (WT) and Rnf144a‐deficient (KO) PMA‐THP1 cells were infected with HSV‐1 (MOI = 1) for the indicated periods. The immunoblot assays were then performed.